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. 2022 Aug 16;11(16):2540. doi: 10.3390/cells11162540

Figure 7.

Figure 7

OGR1 is pro-inflammatory in 16-HBE but not in healthy human fibroblasts. Here, 16-HBE cells were treated with either control (GFP) or OGR1 plasmids followed by treatment with TGF-β, LPS, or CTGF, and secreted IL-6 levels were measured via ELISA. In 16-HBE cells, OGR overexpression alone caused significant IL-6 secretion (A, **** p < 0.0001). As expected, TGF-β, LPS, and CTGF also induced significant IL-6 secretion (A, **** p < 0.0001 for all significant treatment conditions). However, we did not observe an additive or synergistic effect with OGR1 and other cytokines/growth factors. In contrast, OGR1 overexpression did not induce IL-6 secretion in fibroblasts (B). However, TGF-β and LPS did cause significant increases in secreted IL-6 (B, **** p < 0.0001, *** p = 0.0002, ** p = 0.0057), whereas CTGF did not. Interestingly, OGR1 overexpression appears to have no effect on inflammatory signaling in fibroblasts. Open circles represent basal control conditions and closed circles represent OGR1 under basal conditions. Open boxes represent control plasmid plus TGF-β, and closed boxes represent OGR1 plasmid plus TGF-β. Open diamonds represent control plasmid plus LPS, and closed diamonds represent OGR1 plasmid plus LPS. Open upward arrows represent control plasmid plus CTGF, and closed upward arrows represent OGR1 plasmid plus CTGF.